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Mechanisms compensating for dopamine loss in early Parkinson disease
Oleh:
Brotchie, Jonathan
;
Fitzer-Attas, Cheryl
Jenis:
Article from Journal - ilmiah internasional
Dalam koleksi:
Neurology (Official Journal of The American Academy of Neurology) vol. 72 no. 7 Supp 2 (Feb. 2009)
,
page S32-S38.
Topik:
DOPAMINERGIC
;
DEMENTIA
Ketersediaan
Perpustakaan FK
Nomor Panggil:
N11.K.2009.02
Non-tandon:
1 (dapat dipinjam: 0)
Tandon:
tidak ada
Lihat Detail Induk
Isi artikel
Parkinson disease (PD) is a disorder with a substantive period before the emergence of motor symptoms, during which significant dopaminergic neuronal loss is counterbalanced by endogenous compensatory mechanisms. Many potential compensatory mechanisms have now been proposed; these are both dopaminergic, focused on enhancing effects or exposure to existing dopamine, and nondopaminergic, being focused on reducing activity of the indirect striatal output pathway. Compensatory mechanisms can potentially postpone and reduce the severity of parkinsonian symptoms, and contribute to the benefit provided by a symptomatic therapy, thus offering targets for novel therapeutics. However, enhancement of certain compensatory mechanisms may produce problems when subsequent therapies are initiated, e.g., the development of motor complications with levodopa. Supporting endogenous compensatory mechanisms, to delay or reverse apparent disease progression, is a novel and attractive "disease-modifying" approach to PD. Such actions may contribute to the apparent disease-modifying benefit of initiating early treatment with levodopa or rasagiline, as suggested by the ELLDOPA and TEMPO studies.
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